Cardiopulmonary effects of high-impulse noise exposure.

J Trauma

Department of Respiratory Research, Walter Reed Army Institute of Research, Washington, DC, USA.

Published: October 1997

In high-energy impulse noise environments, the biomechanical coupling process between the external forces and the pathophysiology of cardiopulmonary injury is not well understood. A 12-in-diameter compressed air-driven shock tube with reflector plate was used to induce three levels of pulmonary contusion injury in a large animal model. Twenty-one anesthetized sheep were exposed to the various levels of impulse noise generated by the shock tube, with six additional sheep serving as a control group. Pathologic evaluations, performed 3 hours after exposure, showed pulmonary contusion ranging from minor petechial changes on the surface of the lung parenchyma to diffuse ecchymoses affecting as much as 60% of the lung. The gross pathologic observations of injury produced by exposure to the impulse noise produced by the shock tube were similar to those reported for blunt impact trauma or exposure to chemical or grain-dust explosions. The extent of lung injury (lung injury index) was quantitatively assessed. A semilogarithmic relationship between the lung injury index and the measured peak pressure was demonstrated. A significant linear correlation was demonstrated between lung injury index and lung weight-to-body weight ratio. Significant cardiopulmonary changes were also observed as a result of exposure to high-impulse noise. Although in most cases the degree of change was related to the severity of the injury, significant cardiopulmonary function changes were also observed in the absence of significant grossly observable pulmonary injury. Cardiac injury was indicated by decreased cardiac output and hypotension at all levels of injury and might be the result of myocardial contusion or air emboli. Pulmonary injury was demonstrated by respiratory acidosis, increases in lung resistance, and decreases in lung compliance and lung volume. Arterial PO2 appeared to be the most sensitive parameter of injury and was decreased for all measurement intervals for all exposure groups.

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